No abstract

Background: An inappropriate accumulation of fibrillar collagen is a common pathologic feature of early aged hypertensive heart disease, but little information regarding the effects of exercise training on cardiac fibrosis in hypertension is available. The purpose of this study was to evaluate the effects of exercise training on cardiac fibrotic pathways in early aged hypertensive rats. Methods: Masson’s trichrome staining and Western blotting were performed on the excised left ventricle from twenty male spontaneously hypertensive rats at age of 48 weeks, which were randomly divided into either a sedentary hypertensive group (SHR) or exercise hypertensive group (SHR-EX, running on a treadmill running occurred 5 days/week for 60 min/day, for 12 weeks), and from age-matched male Wistar–Kyoto normotensive controls (WKY). Results: Interstitial fibrosis was reduced in the SHR-Ex group when compared with the SHR group. The fibrotic-related protein levels of AT 1 R, FGF23, LOX-2, TGF-β, CTGF, p-Smad 2/3, MMP-2/TIMP-2, MMP-9/TIMP-1, uPA and collagen I were decreased in the SHR-EX group, when compared with the SHR group. Conclusions: Exercise training suppresses early aged hypertensive heart-induced LOX-2/TGF-β-mediated fibrotic pathways associated with decreasing AT 1 R and FGF23, which might provide a new therapeutic effect for exercise training to prevent adverse cardiac fibrosis and myocardial abnormalities in early aged hypertension.

Ching-Hsiang Lai and Ren-Jing Huang share equal contribution. Shin-Da Lee and Hua Ting share equal contribution.

Whole-Body Periodic Acceleration (WBPA) has been reported to induce endothelial nitric oxide and cause vasodilation. However, the effects of WBPA on blood pressure and cardiovascular hemodynamics are still unclear and controversial. The objective of this study was to determine whether a single session of 160-degree V-shape Whole-Body Periodic Acceleration (WBPA-V-160), i.e., periodic motion of the supine body headward to footward, improved blood pressure and cardiovascular parameters. A pre-evaluation and post-evaluation of blood pressure and cardiovascular hemodynamics via DynaPulse Noninvasive and Quantitative Hemodynamic Profile Analysis were performed after a single 30 min trial of WBPA-V-160 with a moving distance, headward to footward, of 2 mm, at a constant frequency of 4 Hz. Systolic BP, diastolic BP, heart rate, end systolic pressure, end diastolic pressure, mean arterial BP, and pulse pressure at post-evaluation were significantly lower than at pre-evaluation after WBPA-V-160, whereas systemic vascular compliance and brachial artery distensibility at post-evaluation were significantly higher than at pre-evaluation. The WBPA-V-160, performed for 30 min, did improve blood pressure and cardiovascular hemodynamics by lowing the BP parameters and enhancing systemic vascular compliance.

Background: The present study investigated whether angiotensin II type 1 receptor blocker irbesartan (ARB) and partial agonist of PPAR-γ prevents heart apoptosis by suppressing cardiac Fas/FasL-mediated to mitochondria-mediated apoptosis in the hearts of hypertensive rat model. Methods: Cardiac function using echocardiography, H&E staining, TUNEL assay, and Western blotting were measured in the excised hearts from three groups, i.e., an untreated hypertensive group (SHR), an ARB-treated hypertensive group (50 mg/kg/day, S.C., SHR-ARB), and untreated normotensive Wistar-Kyoto rats (WKY). Results: Fas Ligand, Fas death receptors, FADD, active caspase-8, active caspase-3 (Fas/FasL-mediated apoptotic pathway), as well as Bax, cytochrome c, active caspase-9 and -3 (mitochondria-mediated apoptotic pathway), IGF-II, and p-JNK were decreased in SHR-ARB group when compared with the SHR group. SIRT1, PGC-1α, Bcl2, and Bcl-xL (SIRT1/PGC-1α pro-survival pathway) were increased in the SHR-ARB group when compared with the SHR group. Conclusions: Our findings suggested that the ARB might prevent cardiac Fas/FasL-mediated to mitochondria-mediated apoptosis pathway in the hypertensive model associated with IGF-II, p-JNK deactivation, and SIRT1/PGC-1α pro-survival pathway upregulation. ARB prevents hypertension-enhanced cardiac apoptosis via enhancing SIRT1 longevity signaling and enhances the mitochondrial biogenetic survival pathway.